S-EPMC6398220 - Microvasculature and intraplaque hemorrhage in atherosclerotic carotid lesions: a cardiovascular magnetic resonance imaging study. - OmicsDI

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Microvasculature and intraplaque hemorrhage in atherosclerotic carotid lesions: a cardiovascular magnetic resonance imaging study.

ABSTRACT: BACKGROUND:The presence of intraplaque haemorrhage (IPH) has been related to plaque rupture, is associated with plaque progression, and predicts cerebrovascular events. However, the mechanisms leading to IPH are not fully understood. The dominant view is that IPH is caused by leakage of erythrocytes from immature microvessels. The aim of the present study was to investigate whether there is an association between atherosclerotic plaque microvasculature and presence of IPH in a relatively large prospective cohort study of patients with symptomatic carotid plaque. METHODS:One hundred and thirty-two symptomatic patients with ?2?mm carotid plaque underwent cardiovascular magnetic resonance (CMR) of the symptomatic carotid plaque for detection of IPH and dynamic contrast-enhanced (DCE)-CMR for assessment of plaque microvasculature. Ktrans, an indicator of microvascular flow, density and leakiness, was estimated using pharmacokinetic modelling in the vessel wall and adventitia. Statistical analysis was performed using an independent samples T-test and binary logistic regression, correcting for clinical risk factors. RESULTS:A decreased vessel wall Ktrans was found for IPH positive patients (0.051?±?0.011?min-?1 versus 0.058?±?0.017?min-?1, p?=?0.001). No significant difference in adventitial Ktrans was found in patients with and without IPH (0.057?±?0.012?min-?1 and 0.057?±?0.018?min-?1, respectively). Histological analysis in a subgroup of patients that underwent carotid endarterectomy demonstrated no significant difference in relative microvessel density between plaques without IPH (n?=?8) and plaques with IPH (n?=?15) (0.000333?±?0.0000707 vs. and 0.000289?±?0.0000439, p?=?0.585). CONCLUSIONS:A reduced vessel wall Ktrans is found in the presence of IPH. Thus, we did not find a positive association between plaque microvasculature and IPH several weeks after a cerebrovascular event. Not only leaky plaque microvessels, but additional factors may contribute to IPH development. TRIAL REGISTRATION:NCT01208025 . Registration date September 23, 2010. Retrospectively registered (first inclusion September 21, 2010). NCT01709045 , date of registration October 17, 2012. Retrospectively registered (first inclusion August 23, 2011).

SUBMITTER: Crombag GAJC

PROVIDER: S-EPMC6398220 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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Microvasculature and intraplaque hemorrhage in atherosclerotic carotid lesions: a cardiovascular magnetic resonance imaging study.

Crombag Geneviève A J C GAJC Schreuder Floris H B M FHBM van Hoof Raf H M RHM Truijman Martine T B MTB Wijnen Nicky J A NJA Vöö Stefan A SA Nelemans Patty J PJ Heeneman Sylvia S Nederkoorn Paul J PJ Daemen Jan-Willem H JH Daemen Mat J A P MJAP Mess Werner H WH Wildberger J E JE van Oostenbrugge Robert J RJ Kooi M Eline ME

Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance 20190304 1

<h4>Background</h4>The presence of intraplaque haemorrhage (IPH) has been related to plaque rupture, is associated with plaque progression, and predicts cerebrovascular events. However, the mechanisms leading to IPH are not fully understood. The dominant view is that IPH is caused by leakage of erythrocytes from immature microvessels. The aim of the present study was to investigate whether there is an association between atherosclerotic plaque microvasculature and presence of IPH in a relatively ...[more]

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Project description:BackgroundIt is unclear whether faster progression of atherosclerosis explains the higher risk of cardiovascular events in CKD. The objectives of this study were to 1. Characterize the associations of CKD with presence and morphology of atherosclerotic plaques on carotid magnetic resonance imaging (MRI) and 2. Examine the associations of baseline CKD and carotid atherosclerotic plaques with subsequent cardiovascular events.MethodsIn a subgroup (N = 465) of Systolic Blood Pressure Intervention Trial. (SPRINT) participants, we measured carotid plaque presence and morphology at baseline and after 30-months with MRI. We examined the associations of CKD (baseline eGFR < 60 ml/min/1.73m2) with progression of carotid plaques and the SPRINT cardiovascular endpoint.ResultsOne hundred and ninety six (42%) participants had CKD. Baseline eGFR in the non-CKD and CKD subgroups were 77 ± 14 and 49 ± 8 ml/min/1.73 m2, respectively. Lipid rich necrotic-core plaque was present in 137 (29.5%) participants. In 323 participants with both baseline and follow-up MRI measurements of maximum wall thickness, CKD was not associated with progression of maximum wall thickness (OR 0.62, 95% CI 0.36 to 1.07, p = 0.082). In 96 participants with necrotic core plaque at baseline and with a valid follow-up MRI, CKD was associated with lower odds of progression of necrotic core plaque (OR 0.41, 95% CI 0.17 to 0.95, p = 0.039). There were 28 cardiovascular events over 1764 person-years of follow-up. In separate Cox models, necrotic core plaque (HR 2.59, 95% CI 1.15 to 5.85) but not plaque defined by maximum wall thickness or presence of a plaque component (HR 1.79, 95% CI 0.73 to 4.43) was associated with cardiovascular events. Independent of necrotic core plaque, CKD (HR 3.35, 95% CI 1.40 to 7.99) was associated with cardiovascular events.ConclusionsPresence of necrotic core in carotid plaque rather than the presence of plaque per se was associated with increased risk of cardiovascular events. We did not find CKD to be associated with faster progression of necrotic core plaques, although both were independently associated with cardiovascular events. Thus, CKD may contribute to cardiovascular disease principally via mechanisms other than atherosclerosis such as arterial media calcification or stiffening.Trial registrationNCT01475747 , registered on November 21, 2011.

Project description:BackgroundIntraplaque hemorrhage (IPH) is associated with plaque progression and ischemic events, and plaque lipid content (% lipid core) predicts the residual atherosclerotic cardiovascular disease risk. This study examined the impact of IPH on lipid content change in the setting of intensive lipid-lowering therapy.MethodsIn total, 214 AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low High-Density Lipoprotein/High Triglycerides: Impact on Global Health Outcomes) participants with clinically established ASCVD and low high-density lipoprotein cholesterol received cartoid MRI at baseline and 2 years to assess changes in carotid morphology and composition. Patients were randomized to extended-release niacin or placebo, and all received simvastatin with optional ezetimibe as necessary to lower low-density lipoprotein cholesterol to 40 to 80 mg/dL. Changes in lipid content and carotid morphology were tested using the Wilcoxon signed-rank test. Differences between subjects with and without IPH and between subjects assigned extended-release niacin or placebo were tested using the Wilcoxon rank-sum test. Linear regression was used to test the association of IPH and lipid content changes after adjusting for clinical risk factors.ResultsAmong 156 patients (61±9 years; 81% men) with complete MRI, prior statin use: <1 year, 26%; 1 to 5 years, 37%; >5 years, 37%. Triglycerides and ApoB decreased significantly, whereas high-density lipoprotein cholesterol and ApoA1 increased significantly over time. Plaque lipid content was significantly reduced (-0.5±2.4 %/year, P = 0.017) without a significant difference between the 2 treatment groups. However, the lipid content increased in plaques with IPH but regressed in plaques without IPH (1.2±2.5 %/year versus -1.0±2.2, P = 0.006). Additionally, IPH was associated with a decrease in lumen area (-0.4±0.9 mm2/year versus 0.3±1.4, P = 0.033). IPH remained significantly associated with increase in lipid content in multivariable analysis (54.4%, 95% CI: 26.8, 88.0, P < 0.001).ConclusionsCarotid plaques under continued intensive lipid-lowering therapy moved toward stabilization. However, plaques with IPH showed greater increases in lipid content and greater decreases in lumen area than plaques without IPH.RegistrationURL: https://www.Clinicaltrialsgov; Unique identifier: NCT01178320.

Project description:BACKGROUND:A three-dimensional (3D) cardiovascular magnetic resonance (CMR) vessel wall imaging (VWI) technique based on 3D T1 weighted (T1w) Sampling Perfection with Application-optimized Contrast using different flip angle Evolutions (SPACE) has recently been used as a promising CMR imaging modality for evaluating extra-cranial and intra-cranial vessel walls. However, this technique is yet to be validated against the current diagnostic imaging standard. We therefore aimed to evaluate the diagnostic performance of 3D CMR VWI in characterizing carotid disease using intra-arterial digital subtraction angiography (DSA) as a reference. METHODS:Consecutive patients with at least unilateral >?50% carotid stenosis on ultrasound were scheduled to undergo interventional therapy were invited to participate. The following metrics were measured using 3D CMR VWI and DSA: lumen diameter of the common carotid artery (CCA) and segments C1-C7, stenosis diameter, reference diameter, lesion length, stenosis degree, and ulceration. We assessed the diagnostic sensitivity, specificity, accuracy, and receiver operating characteristic (ROC) curve of 3D CMR VWI, and used Cohen's kappa, the intraclass correlation coefficient (ICC), and Bland-Altman analyses to assess the diagnostic agreement between 3D CMR VWI and DSA. RESULTS:The ICC (all ICCs ?0.96) and Bland-Altman plots indicated excellent inter-reader agreement in all individual morphologic measurements by 3D CMR VWI. Excellent agreement in all individual morphologic measurements were also found between 3D CMR VWI and DSA. In addition, 3D CMR VWI had high sensitivity (98.4, 97.4, 80.0, 100.0%), specificity (100.0, 94.5, 99.1, 98.0%), and Cohen's kappa (0.99, 0.89, 0.84, 0.96) for detecting stenosis >?50%, stenosis >?70%, ulceration, and total occlusion, respectively, using DSA as the standard. The AUC of 3D CMR VWI for predicting stenosis >?50 and?>?70% were 0.998 and 0.999, respectively. CONCLUSIONS:The 3D CMR VWI technique enables accurate diagnosis and luminal feature assessment of carotid artery atherosclerosis, suggesting that this imaging modality may be useful for routine imaging workups and provide comprehensive information for both the vessel wall and lumen.

Project description:BackgroundBoth stenosis rate and intraplaque hemorrhage (IPH) are important predictors of stroke risk. Simultaneous non-contrast angiography and intraplaque hemorrhage (SNAP) cardiovascular magnetic resonance (CMR) imaging can detect both stenosis rate and IPH. We aimed to evaluate consistency between SNAP and digital subtraction angiography (DSA) to assess symptomatic patients with stroke and explore the performance of SNAP to identify IPH and the clinical factors associated with IPH.MethodsEighty-one symptomatic patients with stroke, admitted to Wuhan Union Hospital who underwent CMR high-resolution vessel wall imaging (HR-VWI) and SNAP, were retrospectively identified. For patients who received interventional therapy, the imaging functions of SNAP and HR-VWI were compared with DSA. The diameters of the intracranial and carotid vessels were measured, and stenotic vessels were identified. The consistency of SNAP and HR-VWI in identifying IPH was also examined, and the correlations between IPH and clinical factors were analyzed.ResultsSNAP was more consistent with DSA than HR-VWI in measuring vascular stenosis (intraclass correlation coefficient [ICC]SNAP-DSA = 0.917, ICC HR-VWI-DSA = 0.878). Regarding the diameter measurements of each intracranial and carotid vessel segment, SNAP was superior or similar to HR-VWI, and both were consistent with DSA in the measurement of major intracranial vascular segments. HR-VWI and SNAP exhibited acceptable agreement in identifying IPH (Kappa = 0.839, 95% confidence interval [CI]: 0.704-0.974). Patients who underwent interventional therapy had a higher plaque burden (P < 0.001). Patients with IPH had lower levels of high-density lipoprotein cholesterol (HDL) (P = 0.038) and higher levels of blood glucose (P = 0.007) and cystatin C (P = 0.040).ConclusionsCMR SNAP is consistent with DSA in measuring vessel diameters and identifying atherosclerosis stenosis in each intracranial and carotid vessel segment. SNAP is also a potential alternative to HR-VWI in identifying stenosis and IPH.

Project description:ImportanceIt remains unknown whether in an asymptomatic community-based cohort magnetic resonance imaging (MRI) measures of plaque characteristics are independently associated with incident cardiovascular disease (CVD) events when adjusted for carotid artery (CA) wall thickness, a measure of plaque burden.ObjectiveTo assess associations of CA MRI plaque characteristics with incident CVD events.Design, setting, and participantsThe Atherosclerosis Risk in Communities (ARIC) study is a prospective epidemiologic study of the incidence of CVD in 15 792 adults of which 2066 women and men were enrolled in the ARIC Carotid MRI substudy. ARIC participants were enrolled from 1987 to 1989, and the substudy was conducted between January 2004 and December 2005. Analysis began January 2017 and ended August 2020.ExposuresIncident CVD events during a median (interquartile range [IQR]) follow-up time of 10.5 (8.1-10.9) years were assessed.Main outcomes and measuresProportional hazards Cox analyses were performed to ascertain associations between MRI variables of CA plaque burden and plaque characteristics.ResultsOf 15 792 ARIC participants, 2066 were enrolled in the substudy, of whom 1256 (701 women [55.8%]) had complete data and were eligible for incident CVD analyses. Carotid artery plaques in participants with incident CVD events (172 [13.7%]) compared with those without (1084 [86.3%]) had a higher normalized wall index (median [IQR], 0.48 [0.36-0.62] vs 0.43 [0.34-0.55]; P = .001), maximum CA wall thickness (median [IQR], 2.22 [1.37-3.52] mm vs 1.96 [1.29-2.85] mm; P = .01), maximum CA stenosis (median [IQR], 5% [0%-22%] vs 0% [0%-13%]; P < .001), and when present, a larger lipid core volume (median [IQR], 0.05 [0.02-0.11] mL vs 0.03 [0.01-0.07] mL; P = .03), respectively. The presence of a lipid core was independently associated with incident CVD events when adjusted for traditional CVD risk factors and maximum CA wall thickness (hazard ratio, 2.48 [95% CI, 1.36-4.51]; P = .003), whereas the presence of calcification was not. The frequency of intraplaque hemorrhage presence in this population of individuals free of CVD at baseline who were not recruited for carotid stenosis was too small to draw any meaningful conclusions (intraplaque hemorrhage presence: 68 of 1256 participants [5.4%]). Carotid artery lumen area and maximum stenosis, which were overall low, were independently associated with incident CVD events when adjusted for traditional CVD risk factors, as anticipated.Conclusions and relevanceThe presence of a CA lipid core on MRI is associated with incident CVD events independent of maximum CA wall thickness in asymptomatic participants.